under reconstruction…

Month: May 2012

Like for many young adults, college was an opportunity to “find” myself and, in particular, connect with my Asian Americanness. In fact, one of the first college courses I enrolled in was Asian American Literature in which one of the prevailing themes in the class was how history and media depicted Asian menas passive, subservient, effeminate or asexual individuals. These emasculated stereotypes would set the stage for my own experience in college, where I learned that masculinity is often measured by how much alcohol you can drink.

It was in this light that I found my own “manhood” challenged because, like many Asians, when I drink my face betrays me. I flush and turn red, often after having just one drink. But while the spectacle of an Asian flushing is not uncommon, in my experience it almost always solicited comments that were variations on one stereotype: Asians can’t drink.

“Cut that Asian kid off.”

“What? You’re already drunk? After one drink? Oh right he’s Asian.”

“He can’t handle drinking. He’s Asian. Look, he’s already red.”

Dismissive and disparaging comments like these accomplished two things: they labelled me as “other” and marked me as less than by some arbitary and artificial measure of masculinity. Worse, though, was that inevitably someone would add insult to injury by trying to explain the biology underlying my deficits…incorrectly.

“It’s because you don’t have the alcohol dehydrogenase gene.”

“Your alcohol dehydrogenase doesn’t work.”

To set the record straight, the “Asian Glow” results from buildup of acetaldehyde, an intermediate of alcohol metabolism. The first step in metabolizing ethanol is its conversion into acetaldehyde by the alcohol dehydrogenase enzyme (ADH1B). Acetaldehyde is, in turn, converted into acetic acid, a reaction catalyzed by the aldehyde dehydrogenase enzyme (ALDH2). Sufferers of alcohol flush syndrome have either a mutation in ADH1B that supercharges the enzyme and dramatically increases the rate that it churns out acetaldehyde from ethanol or a mutation that renders ALDH2 defective in converting acetaldehyde into acetic acid. The consequence of either mutation is the same: a traffic jam of acetaldehyde. The accumulation of acetaldehyde in the system leads to the dilation of capillaries in the face, causing the stereotypical flush. This is followed by early symptoms of hangover such as lightheadedness, nausea, and palpitations– signs indicating that you should probably stop drinking. Carriers of either mutation often feel the effects sooner and more severely.

These undesireable effects might explain the lower incidence of alcoholism amongst East Asian men. After all, why would you keep subjecting yourself to such torture? In fact, these effects mimic to a lesser extent reactions to disulfiram, an inhibitor of ALDH2 activity that is used to treat alcoholism. These mutations in ADH1B and ALDH2 could, therefore, serve as built-in anti-alcoholism mechanisms. Humiliating effects of flushing aside, acetaldehyde also carries with it a significant health risk as it is a known carcinogen. Consistent with this, these mutations in ADH1B and ALDH2 correlate with a higher incidence of esophageal cancer. Furthermore, the mutation in ALDH2 in particular may reduce both the effectiveness of nitroglycerin in treating angina and survival after a heart attack, while increasing the risk for neurodegenerative diseases such as Alzheimer’s.

With these health risks in mind, why would these mutations be so prevalent Asians? From an evolutionary standpoint, the high frequency of these mutations in people of East Asian descent (>59% carry the ADH1B∗47His variant, while approximately 40% carry the ALDH2∗487Lys variant) suggests that these mutations in ADH1B and ALDH2 were positively selected for in recent human history. Why would evolution select for mutations that increase levels of the toxin acetaldehyde? Under what conditions would these mutations provide an evolutionary advantage? And, more importantly, is there an evolutionary basis for drinking wussiness in Asians? While these questions remain unanswered, scientists have proposed several hypotheses. One explanation proposes that the higher concentrations of acetaldehyde resulting from these mutations may act as a defense against infections by parasites that are unable to metabolize acetaldehyde. Alternatively, the adverse reactions to alcohol in individuals with these mutations may have provided greater protection against alcoholism or risks associated with alcohol consumption. For instance, given that alcohol consumption and Hepatitis B virus (HBV) infection can synergistically increase the risk for liver cancer and considering that the geographic distribution of the mutation in ALDH2 overlaps with areas endemic for HBV, the mutation in ALDH2 may have mitigated the effects of HBV infection. Similarly, it has been proposed that sensitivity to alcohol could be a defense mechanism that limits consumption of alcoholic or fermented foods containing toxic or disease-related compounds. All of these hypotheses, however, remain speculative.

While this version of the emasculated Asian male stereotype bothers me on a visceral and instinctual level, I don’t subscribe to this view of masculinity defined by alcohol consumption. There are countless things I’d rather do than trying to prove myself by drinking to oblivion and end up hugging cold, hard porcelain at the end of the night. But I can’t say the same is true for all Asian Americans (women included). Regardless of whether we come to a concrete evolutionary explanation for the prevalence of these mutations, the biology indicates that for a significant number of Asians drinking poses potentially more severe health problems than just alcohol flush, low tolerance, or hangovers alone. These are health concerns that we must keep in mind as Asian Americans conform to a culture that places significant emphasis on drinking, especially in cases where they are pressured into trying to break the stereotype that “Asians can’t drink” because for many of them, they’ll be fighting biology also.

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You could make a case for “looking weird” being an effective survival strategy. Just ask Calvin the lobster whose calico-patterned shell spared it from dining table destiny. Rather than being dunked into a pot of boiling water, Calvin is now on display at the New England Aquarium. Calico-patterned lobsters are extremely rare, occuring about 1 in 30 million. For comparison, the rarest are albino lobsters, which occur at a rate of about 1 in 100 million whereasblue lobsters are more commonly found (~1 in 2 million).

But even stranger looking lobsters are lurking out there in our oceans. Take for instance this two-toned lobster that looks like only one half of it was cooked :

As odd as this lobster looked initially, the more I looked at this picture the more familiar it seemed to me. Where have I seen something like this before? I paced around the lab a bit yesterday and it dawned on me. I’ve seen something like this happen in Drosophila. Every once in a while I’ll find a fruit fly where one half of its body is yellow and other half is brown–split right down the middle. Or more strikingly one eye is white and the other is red. And what’s even more peculiar, one half of the fly will be male with male specific structures like the sex comb and the other half is female. The genitalia of these individuals can vary from having “two complete sets of genitalia, one male, one female. Most of the time, you get weird mish-mashes of tissue that don’t look like male or female genitalia (h/t @DaveMellert).” This bilateral sexual asymmetry is a form of gynandromophy, where an organism abnormally displays both male and female characteristics and is not to be confused with hermaphrodites which are organisms that have both male and female sexual reproductive organs.

Drosophila gynandromorph

In Drosophila, sexis determined using the XX/XY sex-determination system (also used in humans) in which females have 2 X chromosomes and males have 1 X chromosome and 1 Y chromosome. Bilateral gynandromorphy in Drosophila occurs when there is a spontaneous, anomalous loss of an X chromosome during the first mitotic division in a female zygote. This results in one daughter nucleus* containing 2 X chromosomes (denoted as XX) and the other daughter nucleus containing only 1 X chromosome (denoted as XO). In this situation, cells derived from the XX nucleus will give rise to the female body plan in half of the fly while cells derived from the XO nucleus will give rise to the male half despite the lack of a Y chromosome. This is because in Drosophila the most important factor in sex determination is the number of X chromosomes. This phenomena also indicates that by the first mitotic division the left and right side of the Drosophila has been determined since one half will become male and the other female. All of the descendants of one cell will makeup the entire left side of the animal while all the descendants of the other cell will makeup the right side!

XX/XY sex-determination system in Drosophila

Although this explains how bilateral sexual asymmetry occurs, you might be wondering why in the Drosophila gynandromorph above one half of its body is yellow (left) and the other is brown (right) or why one eye is white and the other is red. This is because the genes that determine eye and body color are found on the X chromosome. So in the case of eye color, the original zygote was heterozygous for the gene controlling eye color–it has the recessive allele or gene variant for white eyes (w) on one X chromosome and the wildtype allele for red eyes (w+) on the other X chromosome. During mitosis, one of the w+ -bearing X chromosomes is lost and so cells derived from this XO nucleus will carry only the white eye gene, therefore giving rise to 1 white eye. The other eye is heterozygous for the eye color gene, but since w is recessive the eye will be red by virtue of also carrying the wildtype w+ allele. Of course, loss of the X chromosome can also occur after the first mitotic division, in which case the animal will be a mosaic gynandromorph having patches or regions that are male or female instead of the stark left-right division of male and female body plans.

Gynandromorphy occurs in other animals also, although the specific details depend on the species in question. In butterflies, gynandromorphy is a result of sex chromosome aneuploidy as well but their situation is reversed: XX cells are male and XY or XO cells are female.

In birds, however, gynandromorphy occurs by a different process. Sex determination in birds is different from insects and humans: females have a Z and W chromosome whereas males have 2 Z chromosomes. This chicken is a mosaic of both normal male (ZZ) and female (ZW) cells, with male cells concentrated on 1 side and female cells concentrated on the other.

The exact details of this phenomena in birds is unknown. One hypothesis is that it is due to an error that “occurs in the formation of an egg, which normally carries one chromosome to unite with the single chromosome carried by the sperm. But if an egg accidentally ends up with two chromosomes — a Z and a W — and if this aberrant egg is fertilized by two Z-carrying sperm, the bird that results will have some ZZ cells and some ZW cells, he explained.” Another hypothesis is that the egg is abnormally fertilized by two sperm.

Coming back to lobsters, bilateral gynandromorphs can occur in crustaceans as well. As for humans, however, despite Conrad Lycosthenes’s claims that a bilateral human gynandromorph existed, Natalie Reed explains why this phenomena in all likelihood would not happen, “Back to this not happening in humans: yes, intersexual chimerism can happen in humans. You can even end up with human beings who have one ovary and one testicle. But given that almost all sexual differentiation is a result of hormones, which are more or less evenly distributed throughout the body, you would never see any kind of stark split down the middle of a human with, say, a breast on one side and a flat chest on the other.”

*I say nucleus rather than cells because Drosophila do this strange thing during early embryonic development where the chromosomes duplicate and segregate into separate nuclei without the normal cell division (cytokinesis) that occurs after mitosis. This results in a cell called the syncytial blastoderm that has multiple nuclei without cell membranes separating the nuclei from each other. After 13 rounds of nuclear divisions, cell membranes are finally erected (cellularization) to partition the nuclei into individual cells.

Here is a video of mitosis in the early Drosophila embryo. Note the lack of cell membranes.

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According to 2009 CDC figures, only 27% of male teens (age 15-19) had spoken with their parents about abstinence and contraception. A sobering statistic? Maybe. A surprising one? Not really. I spent a moment of self-reflection and realized that I have never, to this day,spoken with my parents about sex let alone ways to prevent teen pregnancy. Aside from shielding my eyes during sex scenes in a movie, or what my parents called tầm bậy tầm bạ (perverted), they were largely mum on the subject of sex. While some parents advocate avoiding sex, my parents’ collective strategy was to avoid talking about it altogether. I suppose part of the reason was an unspoken expectation that parts of my “education” would be handled by my older brothers. After all, my parents are Vietnamese immigrants, strangers initially to American culture unaccustomed to its norms and values. Their logic was that some things might be better addressed by my brothers, my family’s trailblazers of the American experience. I have three older brothers and only one has made a passing attempt at sexual education: an awkward, mumbling monologue about STD’s before they were called STI’s and to “make sure you use condoms to avoid them.” No mention of how to use them, no demonstration of how to put one on a banana, nothing about getting a girl pregnant. It felt more like an obligation than an education. The reality was that by the time he initiated “the conversation,” I had already been informed. I learned everything, well nearly everything in my 8th grade health class. Where my family failed me, public education prevailed.

I wondered how many other Asian Americans shared my experience growing up sexually uneducated by their parents. I had long inferred that their silence indicated that sex was simply a matter of cultural taboo. A 2006 study of 165 Asian American college students indicated that parents provided minimal education on a range of sexual topics with the least amount of information being provided from fathers to sons. The study also indicated that the students received implicit messages that conveyed strict sexual behavior. Statements such as ‘”romance is for marriage” or that “dating can wait until college” conveyed clear expectations about their children’s sexual conduct without ever explicitly referring to sexual intercourse.’ As to why Asian Americans receive such little sexual information from their parents the authors of the study speculate, “If parents do not initiate these discussions because of the taboo, as was suggested by many of the open-ended responses, then their children may feel that it is not their place to ask such questions. At the same time, a lack of shared vocabulary or difficulty in expressing complex ideas may also create obstacles to intergenerational knowledge or values transmission in some immigrant families.”

Despite this lack of sexual education, the birth rate for Asian American teens remains the lowest amongst all ethnicities (teen birth rate across that board has decreased to historic lows). I was unable to find abortion statistics specifically for Asian American teens, however it has been reported that for Asian American women the percentages of pregnancies that end in abortion is 35% (compared to 18% for white women).

Although the rates of STD’s (gonorrhea, chlamydia, and syphillis) in the Asian American population at large is also lower than other ethnicities–some of which could be due to underreporting, a review of the CDC’s statistical data by Professor Hyeouk Chris Hahm suggests, “that Asian American young women are at risk of high STDs. For instance, Asian American women had a higher prevalence of STDs than White women in both 1995 (10.4% vs. 7.7) and 2001 (13.5% vs. 8.3%). The incidence of STDs (not diagnosed with STDs in 1995, but developed STIs in 2001) among Asian American women was also higher than that of White women.” Slightly dated figures I know but what follows is cause for concern. Alarmingly, the rate of HIV infection has been steadily increasing in the Asian American community. As the Banyan Tree Project reports, “Recent analysis of data from the Centers for Disease Control and Prevention reveals that Asians and Pacific Islanders (A&PIs) have the highest rate of increase in new HIV infections in the nation, the only statistically significant growth among any racial or ethnic group. Though HIV is still seen as a men’s issue, the rate of increase for A&PI women is actually higher than that of A&PI men.” Confounding this issue is that Asian Americans are least likely among all ethnic groups to be tested for HIV.

Whether the increase in STD rates but low teen birth rates for Asian Americans can be directly attributed to the lack of explicit sexual education they receive from their parents is unclear. But as Professor Hahm notes, “Forty years from now, Asian Americans are projected to be 11 percent of the national population. That could be a huge number of STD cases, in addition to related infections such as HIV/AIDS. It’s a potential disaster for public health. We need to understand the problem and create an intervention that works for these communities.” I don’t know if “disaster” is the right characterization, but it is an issue worth our attention where not talking about sex with our Asian American children may prove to be as effective as covering their eyes during a movie’s tầm bậy tầm bạ scenes.

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Yesterday, Jesse Bering, author of The Belief Instinct, gave our weekly departmental seminar. His lecture titled “Is God Just in Your Head? Cognitive Science and the ‘Big Questions'” dealt with concepts in cognitive science that underpin three major existential questions: What is the purpose of life? What should I do (when faced with a choice)? And what happens after I die? Admittedly, I had anticipated a seminar that gave more of an evolutionary perspective as to why we ask these types of questions, but as he disclaimed, “I am not a biologist. This will be a cognitive science talk.” He argued that two connected concepts, the theory of mind, which is the ability to place oneself in “other’s shoes” (including God’s) and teleo functional thinking, “which is reasoning about the functional purpose of an entity or object in question,” are fundamental in understanding “how” we are able to ask these questions.

You can read my live tweets from his talk on Storify. I apologize in advance if I fell short in doing his seminar justice–cognitive science proved to be a more difficult beast to live tweet than the more familiar topics of genetics and molecular biology. Please alert me to anything that I got wrong. I’ll try to get out a more polished blog post within the next few days. And as always, please check out Katie PhD’s lovely sketchnote of Jesse Bering’s talk: